Abstract

In many mammals the ventilatory response to hypoxia depends on ambient temperature (Ta), largely because of the hypometabolic effects of hypoxia below thermoneutrality. We questioned whether the ventilatory response to asphyxia also depends upon Ta, and the role played by metabolism and body temperature (Tb). Oxygen consumption ( V ̇ O 2 ) and pulmonary ventilation (V̇ e) were measured in conscious rats at Ta=27°C (warm) and 11°C (cold), breathing air or two levels of asphyxic gases, moderate (10% O 2–4% CO 2), or severe (10% O 2–8% CO 2), for ≈30 min each. In the cold, the pattern of the V̇ e response to moderate asphyxia was qualitatively similar to that seen in hypoxia alone, i.e the attained V ̇ e / V ̇ O 2 was similar in warm and cold conditions, with, in the latter, a major drop in V ̇ O 2 and little or no hyperpnea. During severe asphyxia, however, the V ̇ e / V ̇ O 2 attained in the cold was less than in the warm, and it was accompanied by a large drop in Tb (≈6°C). Blood gases confirmed the lower asphyxic hyperventilation in the cold. By maintaining Tb at 38°C with an implanted abdominal heat exchanger, the V ̇ e / V ̇ O 2 levels attained during asphyxia were the same between cold and warm conditions. We conclude that (a) the V̇ e response to asphyxia is Ta-dependent, largely because of the hypometabolic effect of the hypoxic component in the cold, (b) during moderate asphyxia the hypercapnic component is qualitatively unimportant, and (c) with severe asphyxia the hypercapnia becomes an important contributor to the Ta-sensitivity by aggravating the decrease in Tb in the cold and lowering V̇ e sensitivity.

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